ArticleClinical and experimental immunology2002
Placentally derived prostaglandin E2 acts via the EP4 receptor to inhibit IL-2-dependent proliferation of CTLL-2 T cells.
Article in Clinical and experimental immunology, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 50 citations in OpenAlex.
- Treatment of cancer-associated fibroblast-like cells with celecoxib enhances the anti-cancer T helper 1/Treg responses in breast cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Amphiregulin orchestrates the paracrine immune-suppressive function of amniotic-derived cells through its interplay with COX-2/PGEiScience · 2024Article
- Protective effects of extracts fromFrontiers in pharmacology · 2023Article
- Cooperative inflammation: The recruitment of inflammatory signaling in marsupial and eutherian pregnancy.Journal of reproductive immunology · 2020Review
- Decidual stromal cell-derived PGEAmerican journal of reproductive immunology (New York, N.Y. : 1989) · 2018Article
- Cardiosphere-derived cells suppress allogeneic lymphocytes by production of PGE2 acting via the EP4 receptor.Scientific reports · 2018Article
- Regulatory T-cells in pregnancy: historical perspective, state of the art, and burning questions.Frontiers in immunology · 2014Review
- EP4 and EP2 receptor activation of protein kinase A by prostaglandin E2 impairs macrophage phagocytosis of Clostridium sordellii.American journal of reproductive immunology (New York, N.Y. : 1989) · 2014Article
- T CD3+CD8+ lymphocytes are more susceptible for apoptosis in the first trimester of normal human pregnancy.Journal of immunology research · 2014Article
- Intrauterine group A streptococcal infections are exacerbated by prostaglandin E2.Journal of immunology (Baltimore, Md. : 1950) · 2013Article
- Postpartum group a Streptococcus sepsis and maternal immunology.American journal of reproductive immunology (New York, N.Y. : 1989) · 2012Review
- Role of cAMP in the promotion of colorectal cancer cell growth by prostaglandin E2.BMC cancer · 2008Article
- Respiratory Francisella tularensis live vaccine strain infection induces Th17 cells and prostaglandin E2, which inhibits generation of gamma interferon-positive T cells.Infection and immunity · 2008Article
- The Th1/Th2 paradigm: still important in pregnancy?Seminars in immunopathology · 2007Review
- Mechanisms underlying the relaxation response induced by bradykinin in the epithelium-intact guinea-pig trachea in vitro.British journal of pharmacology · 2005Article
- Expression of cyclooxygenase-2 in colorectal cancer and its clinical significance.World journal of gastroenterology · 2005Article
- Cyclooxygenase-2 expression and angiogenesis in colorectal cancer.World journal of gastroenterology · 2003Article
Corrections and comments
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Authors and funding
11 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A number of immunomodulatory molecules are present in the placenta, including cytokines, prostaglandins, progesterone and indoleamine 2,3-dioxygenase. An undefined factor capable of down-regulating T-cell activity has recently been reported [1] as being produced by short-term cultures of placental fragments. By careful repetition of these studies we have confirmed that chorionic villi isolated from term placenta produce a low molecular weight, heat stable factor capable of inhibiting the IL-2-dependent proliferation of mouse CTLL-2 cells. This activity was not due, however, to a previously unknown immunosuppressive molecule, but rather to prostaglandin E2 (PGE2). Expression of cyclooxygenase (COX)-2 was detected in the syncytiotrophoblast of chorionic villi explants using immunohistochemistry. Culture of the explants in the presence of the COX-1/COX--2 inhibitors indomethacin and diclofenac, or with the COX-2-selective inhibitor DFP, blocked the production of the immunosuppressive factor. The immunosuppressive activity was restored by adding PGE2 to the supernatants obtained from diclofenac-inhibited explants. A number of different receptors are involved in mediating the biological effects of prostaglandins. By utilizing selective antagonists of individual receptors, we have established that the immunosuppressive effect of PGE2 on CTLL-2 cells is exerted via the EP4 receptor. Thus, addition of an EP4-selective antagonist, but not of EP1 or EP3 antagonists, abolished the immunosuppressive effect of PGE2 on CTLL-2 cells. This may have implications for attempts to selectively manipulate T-cell responses.
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